Regulatory Effects of HMG CoA Reductase Inhibitor and Fish Oils on Apolipoprotein B-100 Kinetics in Insulin-Resistant Obese Male Subjects With Dyslipidemia

Chan, Dick C.; Watts, Gerald F.; Barrett, P. Hugh R.; Beilin, Lawrence J.; Redgrave, Trevor G.; Mori, Trevor A.

doi:10.2337/diabetes.51.8.2377

Cited by 152 publications

(111 citation statements)

References 53 publications

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“…VLDL, IDL, and LDL were isolated from 3 ml plasma by sequential ultracentrifugation (Optima XL-100K; Beckman Coulter, Fullerton, Australia) at densities of 1.006, 1.019, and 1.063 g/ml, respectively. The procedures for isopropranol precipitation, delipidation, hydrolysis, and derivatization of apoB to the oxazolinone derivative were described previously (9,30). Plasmafree leucine was also isolated by cation-exchange chromatography using AG 50 W-X8 resin (BioRad, Richmond, CA) after removing plasma proteins with 60% perchloric acid.…”

Section: Subjectsmentioning

confidence: 99%

“…Quantification of apoB, apoAI, and other analytes. Plasma aliquots were combined to yield five pooled VLDL, IDL, and LDL samples per patient study, as described previously (30). ApoB was isolated in each lipoprotein fraction using isopropanol and quantitated with the Lowry method (9,30).…”

Section: Subjectsmentioning

confidence: 99%

“…Plasma aliquots were combined to yield five pooled VLDL, IDL, and LDL samples per patient study, as described previously (30). ApoB was isolated in each lipoprotein fraction using isopropanol and quantitated with the Lowry method (9,30). Four aliquots of plasma from 4 separate days were pooled to assay HDL apoAl concentration, which was measured as plasma apoAl concentration, assuming that Ͼ90% of apoAl resides in the HDL fraction (31).…”

Section: Subjectsmentioning

confidence: 99%

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Differential Regulation of Lipoprotein Kinetics by Atorvastatin and Fenofibrate in Subjects With the Metabolic Syndrome

et al. 2003

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The metabolic syndrome is characterized by insulin resistance and abnormal apolipoprotein AI (apoAI) and apolipoprotein B-100 (apoB) metabolism that may collectively accelerate atherosclerosis. The effects of atorvastatin (40 mg/day) and micronised fenofibrate (200 mg/day) on the kinetics of apoAI and apoB were investigated in a controlled cross-over trial of 11 dyslipidemic men with the metabolic syndrome. ApoAI and apoB kinetics were studied following intravenous d 3 -leucine administration using gas-chromatography mass spectrometry with data analyzed by compartmental modeling. Compared with placebo, atorvastatin significantly decreased (P < 0.001) plasma concentrations of cholesterol, triglyceride, LDL cholesterol, VLDL apoB, intermediate-density lipoprotein (IDL) apoB, and LDL apoB. Fenofibrate significantly decreased (P < 0.001) plasma triglyceride and VLDL apoB and elevated HDL 2 cholesterol (P < 0.001), HDL 3 cholesterol (P < 0.01), apoAI (P ‫؍‬ 0.01), and apoAII (P < 0.001) concentrations, but it did not significantly alter LDL cholesterol. Atorvastatin significantly increased (P < 0.002) the fractional catabolic rate (FCR) of VLDL apoB, IDL apoB, and LDL apoB but did not affect the production of apoB in any lipoprotein fraction or in the turnover of apoAI. Fenofibrate significantly increased (P < 0.01) the FCR of VLDL, IDL, and LDL apoB but did not affect the production of VLDL apoB. Relative to placebo and atorvastatin, fenofibrate significantly increased the production (P < 0.001) and FCR (P ‫؍‬ 0.016) of apoAI. Both agents significantly lowered plasma triglycerides and apoCIII concentrations, but only atorvastatin significantly lowered (P < 0.001) plasma cholesteryl ester transfer protein activity. Neither treatment altered insulin resistance. In conclusion, these differential effects of atorvastatin and fenofibrate on apoAI and apoB kinetics support the use of combination therapy for optimally regulating dyslipoproteinemia in the metabolic syndrome. Diabetes 52:803-811, 2003

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Section: Subjectsmentioning

confidence: 99%

Section: Subjectsmentioning

confidence: 99%

Section: Subjectsmentioning

confidence: 99%

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Differential Regulation of Lipoprotein Kinetics by Atorvastatin and Fenofibrate in Subjects With the Metabolic Syndrome

et al. 2003

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“…Davidson et al (96) found that after treating HC patients with n-3 PUFA and/or simvastatin for 12 weeks, the TAG responses were similar in the EPA/DHA-group (2 25·3 %) and the combined group (2 28·8 %), and borderline significantly lower in the simvastatin group (2 18·5 %), whereas decreases in non-HDL-cholesterol and increases in HDL-cholesterol were statistically significant only for the combined (non-HDL: 2 24·8 %, HDL: þ10·4 %) and simvastatin group (non-HDL: 2 25·8 %, HDL: þ7·2 %). All other studies found significant improvements of TAG with a combination therapy compared with the statin therapy alone (94,95,97,99,104) . Study populations included, besides HC patients, renal transplant patients with persistent hypercholesterolaemia (99) and insulin-resistant obese men with dyslipidaemia (95) .…”

Section: Effects Of Combination Therapy With N-3 Pufa and Statinsmentioning

confidence: 93%

“…The authors suggest that the two compounds reduce TAG levels through different mechanisms. Whereas n-3 PUFA reduced the hepatic secretion of VLDL-apoB, atorvastatin enhanced the clearance of all apo B-containing lipoproteins, resulting in an additive effect (94,95) . Aligeti et al performed a retrospective cohort study in which they compared the change in plasma TAG levels between patients taking fish oil as monotherapy and patients who added fish oil to their usual lipid-lowering Table 7.…”

Section: Effects Of Combination Therapy With N-3 Pufa and Statinsmentioning

confidence: 99%

Support of drug therapy using functional foods and dietary supplements: focus on statin therapy

et al. 2010

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Functional foods and dietary supplements might have a role in supporting drug therapy. These products may (1) have an additive effect to the effect that a drug has in reducing risk factors associated with certain conditions, (2) contribute to improve risk factors associated with the condition, other than the risk factor that the drug is dealing with, or (3) reduce drug-associated side effects, for example, by restoring depleted compounds or by reducing the necessary dose of the drug. Possible advantages compared with a multidrug therapy are lower drug costs, fewer side effects and increased adherence. In the present review we have focused on the support of statin therapy using functional foods or dietary supplements containing plant sterols and/or stanols, soluble dietary fibre, n-3 PUFA or coenzyme Q 10 . We conclude that there is substantial evidence that adding plant sterols and/or stanols to statin therapy further reduces total and LDL-cholesterol by roughly 6 and 10 %, respectively. Adding n-3 PUFA to statin therapy leads to a significant reduction in plasma TAG of at least 15 %. Data are insufficient and not conclusive to recommend the use of soluble fibre or coenzyme Q 10 in patients on statin therapy and more randomised controlled trials towards these combinations are warranted. Aside from the possible beneficial effects from functional foods or dietary supplements on drug therapy, it is important to examine possible (negative) effects from the combination in the long term, for example, in post-marketing surveillance studies. Moreover, it is important to monitor whether the functional foods and dietary supplements are taken in the recommended amounts to induce significant effects. Combination therapy: Dyslipidaemia: Statins: Functional foodsThe world market for functional foods (FF) and dietary supplements (DS) is expanding rapidly. In 2010 FF are expected to represent 5 % of the total global food market (1) and the market for DS is estimated at more than $60 billion worldwide (2) . In general, the target population of FF or DS is healthy individuals with slightly elevated risk factors or some physical discomfort. However, due to the fast growing market of FF or DS and the accompanying strong advertising and marketing, also patients on medication may be stimulated to use FF or DS. This may have several consequences for the quality of drug treatment as stated by de Jong et al. with the example of the combined intake of plant sterols and/or stanols and statins (3) . Whereas they addressed the additive effect of plant sterols and/or stanols on reducing LDL-cholesterol values in patients on statin treatment, their main focus was the possible negative aspects of the combination, such as unfavourable effects on patient adherence with drug treatment and increasing the potential for food-drug interactions.In the present review we will focus on the possible beneficial effects that FF or DS may have on drug therapy. Because of the large number of subjects treated suboptimally with statins (hydroxymethylglutaryl Co...

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Lipid lowering efficacy of atorvastatin

Adams

Tsang

Wright

2012

Cochrane Database of Systematic Reviews

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Regulatory Effects of HMG CoA Reductase Inhibitor and Fish Oils on Apolipoprotein B-100 Kinetics in Insulin-Resistant Obese Male Subjects With Dyslipidemia

Cited by 152 publications

References 53 publications

Differential Regulation of Lipoprotein Kinetics by Atorvastatin and Fenofibrate in Subjects With the Metabolic Syndrome

Differential Regulation of Lipoprotein Kinetics by Atorvastatin and Fenofibrate in Subjects With the Metabolic Syndrome

Support of drug therapy using functional foods and dietary supplements: focus on statin therapy

Lipid lowering efficacy of atorvastatin

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